Author: T. Malik and D.J. Haleem

Introduction: HAL elicits NAS along Parkinsonism. HAL induces c-Fos responsiveness in a distributed anxiety-related neural scheme, selected neuronal population of nucleus accumbens. Mood deficits by HAL metabolically effect via diet restriction that reduced body weight. GTE is known to control appetite and body weight while exerting anxiolytic effects. Aim: The current study testifies the hypothesis that GTE may control HAL elicited NAS with reducing Parkinsonism. Methods: Rats (n=6) were treated with one of the four treatments; oral fluid [water/GTE (1 gm/liter)] plus saline; or oral fluid plus i.p HAL (1 mg/kg/day) administration. Behavioral assessments and neurochemical analysis were performed following six weeks of treatments. Results: suggest that HAL induced decreases in fluid, food intake and growth rate were greater in GTE treated animals. GTE was shown to induce anxiogenic behavior examined in light dark box transitional test but not in fear like exploratory behavior on elevated plus maze and motor deficits on rota rod performance. HAL induced locomotor activity was suppressed, innate aversive and fear like exploratory behaviors were greater in GTE than water drinking animals. HAL induced serotonergic metabolism was increased in the caudate and nucleus accumbens and decreased in the serotonin availability in the rest of the brain regions of GTE treated animals. HAL induced decreased dopamine was increase din the nucleus accumbens of GTE drinking than water drinking animals. Conclusion: Potential mechanism involved in the greater anorexiogenic effects of GTE and greater HAL induced NAS plus Parkinsonism in GTE treated animals is proposed for demonstration in this meeting.